EVENT ABSTRACTS
Acute kidney injury (AKI) is a common complication after cardiac surgery with cardiopulmonary bypass (CPB) occurring in about 22% of patients, significantly increasing morbidity and mortality post-operatively. Patient-related risk factors increasing AKI risk include age, preexisting heart or kidney disease, hypertension, diabetes, atherosclerosis and medications taken, such as aspirin or angiotensin-converting enzyme (ACE) inhibitors. CPB-related risks are time on CPB during surgery, activation of coagulation, complement and fibrinolysis systems, causing an augmented inflammatory response, kidneys oxygen demand vs. supply mismatch due to haemodilution, decreased mean arterial pressure, increased renal vascular resistance on CPB and glycocalyx shedding on bypass allowing endothelial cell-activated blood interaction. Currently, AKI is defined by serum creatinine level change and urine output, while some novel markers like neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and cell cycle arrest biomarkers have been proposed to quantify renal tubular damage, all failed to elicit high sensitivity and specificity performance. A landmark study demonstrated that systemic delivery of oxygen (DO2) lower than 272ml/min/m2 is strongly associated with AKI in CPB, and a more recent study identified 300ml/min/m2 as a cut-off value for AKI development. A promising study indicated the use of renal NIRS which transcutaneously measures regional oxygenation in kidney area, as an early warning of AKI in CPB, with renal NIRS values lower than 70%,65%,60% and 55% and decline from baseline by 15%,20%,25% and 30% significantly correlating with AKI after CPB surgery. Subsequent renal NIRS validation study confirmed ability of renal NIRS to detect renal vein oxygen saturation in CPB. The study proposed here aims to evaluate if the continuous measurement of DO2 combined with renal NIRS can predict AKI better than DO2 alone and if renal NIRS can be increased by altering MAP or flow. Early signs of kidney hypoxia may buy more time, potentially allowing early intervention during CPB to restore oxygenation.
I currently serve as a Clinical Perfusionist at Bristol Royal Infirmary, where I am dedicated to advancing patient care through innovative perfusion practices. My journey into perfusion began with a solid foundation in nursing, having earned a bachelor’s degree in nursing in 2009 in Lithuania. In 2022, I embarked on a new chapter as a Trainee Perfusionist at the Bristol Royal Infirmary, officially completing the clinical training program in September 2024. Now, as a Clinical Perfusionist, I am particularly focused on research and practices that aim to mitigate acute kidney injury (AKI) associated with cardiopulmonary bypass (CPB).
